ACUTE MYOCARDIAL INFARCTION CLINICAL THERAPEUTICS | PRELIMS (1st Sem)

Case#3
Dr. Magnolia Reyes
September 11, 2020

OUTLINE A. DEFINITION OF TERMS

I. CASE DISCUSSION • ACUTE CORONARY SYNDROME: Spectrum of
A. Definition of Terms acute cardiac ischemia ranging from unstable angina
B. Pathophysiology (ischemic pain at rest or at lower threshold of exertion
II. DIAGNOSTIC CRITERIA FOR ACUTE MI or new onset of chest pain) to acute MI (death of
A. History cardiac tissue), usually precipitated by thrombus
B. Physical findings formation in a coronary artery with an atherosclerotic
C. Electrocardiogram plaque.
D. Cardiac Biomarkers • ACUTE MYOCARDIAL INFARCTION: Death of
E. Diagnosis of MI myocardial tissue because of inadequate blood flow.
F. Differential diagnosis • NON–ST-SEGMENT ELEVATION MYOCARDIAL
III. TREATMENT OF ACUTE MI INFARCTION (NSTEMI): It has other ECG changes,
IV. COMPLICATIONS, RISKS, PREVENTION OF AMI such as ST-segment depression or T-wave
A. Complications of Acute MI inversion. NSTEMI will have elevated cardiac
B. Cardiac Pump Failure and Cardiogenic Shock biomarkers. The pathophysiology is subendocardial
C. Mechanical Problems within the first week ischemia and can cause cardiac muscle dysfunction
D. Late Complications after weeks of MI and shock.
E. Post – MI Risk Stratification • ST-SEGMENT ELEVATION MYOCARDIAL
F. Secondary Prevention of Ischemic Heart INFARCTION (STEMI): ST-segment elevation more
Disease than 0.1 mV in two or more contiguous leads, and
V. Appendix elevated cardiac biomarkers. STEMI has the
pathophysiology of transmural cardiac muscle
ischemia and can therefore cause cardiac
dysfunction and pump failure (cardiogenic shock)
I. CASE DISCUSSION acutely.
A 58-year-old man comes to the emergency • PCI: Percutaneous coronary intervention (angioplasty
department (ED) complaining of chest discomfort. He and/ or stenting).
describes the discomfort as a severe, retrosternal pressure • THROMBOLYTICS: Drugs such as tissue
sensation that had awakened him from sleep 3 hours earlier. plasminogen activator (tPA), streptokinase, and
He previously had been well but has a medical history of reteplase (recombinant plasminogen activator [r-PA]),
hypercholesterolemia and a 40-pack-year history of smoking. which act to lyse fibrin thrombi in order to restore
patency of the coronary artery when PCI is
Physical Examination: The patient appears contraindicated or is not available.
uncomfortable and diaphoretic, with a heart rate of 116 bpm,
blood pressure of 166/102 mm Hg, respiratory rate of 22 B. PATHOPHYSIOLOGY
breaths per minute, and oxygen saturation of 96% on room air. • Usually are caused by in situ thrombosis at the
Jugular venous pressure appears normal. Lungs are normal, site of a ruptured atherosclerotic plaque in a
regular rhythm with S4 gallop no murmur or rubs. Chest X-Ray coronary artery.
shows clear lungs and normal cardiac silhouette. The • Occasionally, they are caused by embolic
electrocardiogram (ECG) is shown in Figure 1. occlusion, coronary vasospasm, vasculitis,
aortic root or coronary artery dissection, or
cocaine use--which promotes both vasospasm
and thrombosis.
• Clinical syndrome is related to both the degree of
atherosclerotic stenosis in the artery and to the
degree of pain depends on duration and extent of
sudden thrombotic occlusion of the artery.
• If there is incomplete Occlusion or if the
thrombus undergoes spontaneous lysis,
unstable angina occurs.
• If there is complete occlusion and pain
remains for more than 30 min myocardial
infarction occurs.

II. DIAGNOSTIC CRITERIA FOR ACUTE MI

A. HISTORY
• Chest pain is the cardinal feature of MI, even
Figure 1. Electrocardiogram result of the patient though it is not universally present. It is of the
same character as angina pectoris—described as
heavy, squeezing, or crushing—and is
localized to the retrosternal area or

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 Prelims (1st Sem) Acute Myocardial Infarction
Dr. Magnolia Reyes
PATHOLOGY· September 11, 2020

epigastrium, sometimes with radiation to the 1. The earliest changes are tall, positive, hyperacute T
arm, lower jaw, or neck. waves in the ischemic vascular territory.
• In contrast to stable angina, however, it persists 2. This is followed by elevation of the ST segments
for more than 30 minutes and is not relieved (myocardial “injury pattern”).
by rest. 3. Over hours to days, T-wave inversion frequently
• The pain often is accompanied by sweating, develops.
nausea, vomiting, and/ or the sense of impending 4. Finally, diminished R-wave amplitude or Q waves
doom. occur, representing significant myocardial necrosis
• In a patient older than 70 years or who is and replacement by scar tissue, and they are what
diabetic, an acute MI may be painless or one seeks to prevent in treating the acute MI
associated with only vague discomfort, but it may
be heralded by the sudden onset of dyspnea, • Sometimes when acute ischemia is limited to
pulmonary edema, or ventricular arrhythmias. the subendocardium, ST-segment
depression, rather than ST-segment
elevation, develops.
• ST-segment elevation is typical of acute
transmural ischemia, that is, a greater
degree of myocardial involvement than in
NSTEMI.
• From the ECG we can localize the
ischemia related to a vascular territory
supplied by one of the three major
coronary arteries.
• As a general rule:

B. PHYSICAL FINDINGS

• There are no specific physical findings in a

patient with an acute MI.
• Many patients are anxious and diaphoretic.
• Cardiac auscultation may reveal an S4 gallop,
reflecting myocardial noncompliance because
of ischemia; an S3 gallop, representing severe
systolic dysfunction;
• New apical systolic murmur of mitral regurgitation
caused by ischemic papillary muscle dysfunction

C. ELECTROCARDIOGRAM
• The ECG is often critical in diagnosing acute MI
and guiding therapy.

D. CARDIAC BIOMARKERS
Cardiac biomarkers- proteins; released into blood
from necrotic heart muscle after an acute MI. (Appendix A)

E. DIAGNOSIS OF MI
The diagnosis of acute MI is made by finding at least
two of the following three features:

1. Typical chest pain persisting for more than 30 minutes

2. Typical ECG findings
3. And elevated cardiac biomarker levels.
F. DIFFERENTIAL DIAGNOSIS
During the initial evaluation, one must consider and
exclude other diagnoses that typically present with chest
pain but would be worsened by the anticoagulation or
thrombolysis usually used to treat acute MI

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 Prelims (1st Sem) Acute Myocardial Infarction
Dr. Magnolia Reyes
PATHOLOGY· September 11, 2020

• Sustained VT (>30 seconds) and VF are life

threatening because they prevent coordinated
ventricular contraction, cause pulselessness and
Aortic dissection Unequal pulses or blood cardiovascular relapse.
pressures in the arms, a new o Treatment: Defibrillation and IV anti-
murmur of aortic insufficiency, arrhythmic drugs (Amiodarone)
or a widened mediastinum on o Check electrolytes: Hypokalemia and
chest x-ray film. Hypomagnesaemia- potentiate ventricular
Acute pericarditis Presents with chest pain and a arrhythmias
pericardial friction rub, but the • Accelerated idioventricular rhythm- benign
ECG findings show diffuse ST- ventricular arrhythmia not suppressed by
segment elevation rather than antiarrhythmics; a wide complex escape rhythm
those limited to a vascular between 60 and 110 bpm; accompanies reperfusion
territory of the myocardium but causes no hemodynamic
compromise
• Sinus bradycardia is frequently seen in inferior MI
III. TREATMENT OF ACUTE MI because the right coronary artery supplies the
sinoatrial node, but the condition generally requires
INITIATED THERAPIES no treatment unless it causes hypotension.
a. Acute thrombosis o If the rate is slow enough to cause cardiac output
i. Antiplatelet – aspirin and blood pressure to fall, intravenous atropine
ii. Anticoagulants – heparin usually is administered.
b. Reduce myocardial demands and limit infarct • Bradyarrhythmia can be cause by Atrioventricular
size (AV) conduction disturbances. Produces widened
i. Beta blockers- decrease myocardial QRS complex
oxygen demand • If in cardiogenic shock from complete heart block will
c. Increase coronary blood flow require a temporary/permanent pacemaker
i. Nitrates
d. To reduce pain B. Cardiac Pump Failure and Cardiogenic Shock
i. Morphine
e. Reduce pain and tachycardia o Cardiogenic shock in acute MI usually is the
i. Oxygen most severe form of left ventricular (LV) pump
✓ Percutaneous coronary intervention (PCI) is the failure manifested by end-organ hypoperfusion.
preferred therapy for most patients, as it is more o Ischemic reduction in ventricular diastolic
effective than fibrinolysis in opening occluded arteries, compliance may lead to transient pulmonary
and is associated with better clinical outcomes congestion, associated with elevated left-sided
✓ Individuals with ST segment elevation benefits from filling pressures.
thrombolytics Myocardium should be salvaged o Cardiogenic shock is diagnosed when: the
before it is irreversibly injured (time is muscle) patient has hypotension with systolic arterial
✓ Thrombolysis should be given within 1-3 hours of pressure less than 80 mm Hg, markedly
onset of chest pain reduced cardiac index less than 1.8 L/min/m2
✓ The major risk of thrombolysis is bleeding and elevated LV filling pressure (measured
✓ The risk is constant; the risk outweighs the benefit by indirectly with a pulmonary capillary wedge
12 hours. At this time, infarctions are completed, the pressure >18 mm Hg).
myocardium is dead o Appear hypotensive cold extremities due to
peripheral vasoconstriction, pulmonary edema
Thrombolytic therapy is indicated if all of the following
and elevated jugular venous pressure
criteria are met:
o Supportive treatment: hemodynamic monitoring,
1. Clinical complaints are consistent with ischemic-type
adequate ventilation and oxygenation, blood
chest pain.
pressure support with vasopressors such as
2. ST-segment elevation more than 1 mm in at least two
dobutamine and dopamine. May require urgent
anatomically contiguous
revascularization with primary Percutaneous
3. There are no contraindications to thrombolytic therapy.
Intervention (PCI) or Coronary Artery Bypass
4. Patient is younger than 75 years (greater risk of
Surgery (CABGS)
hemorrhage if >75).

A. ALGORITHM FOR ASSESMENT AND TREATMENT C. Mechanical Problems within the first week
(APPENDIX B)
• The most common is papillary muscle dysfunction
IV.COMPLICATIONS, RISKS, PREVENTION OF ACUTE MI caused by LV ischemia or infarction, leading to mitral
A. COMPLICATIONS OF ACUTE MI regurgitation
• Mortality in acute MI usually is a result of • papillary muscle rupture, which produces a flail
ventricular arrhythmias, or myocardial pump mitral leaflet and acute mitral regurgitation with
failure and resultant cardiogenic shock. development of heart failure and cardiogenic shock
• Ventricular tachycardia (VT) and Ventricular fibrillation with holosystolic murmur
(VF) occurs in the first 24 hours of MI • rupture of the ventricular free wall, most
catastrophic mechanical complication; as the blood

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 Prelims (1st Sem) Acute Myocardial Infarction
Dr. Magnolia Reyes
PATHOLOGY· September 11, 2020

fills the pericardium, cardiac tamponade develops

rapidly, with sudden pulselessness, hypotension, and
loss of consciousness and almost fatal.

D. Late Complications after weeks of MI

• Ventricular aneurysm, which should be suspected if

ST-segment elevation persists weeks after the event
• Dressler syndrome, an immune phenomenon
characterized by pericarditis, pleuritis, and fever.
This may remit and relapse
o treated with anti-inflammatory drugs, including
nonsteroidal anti-inflammatory drugs
(NSAIDs) and sometimes prednisone.

E. Post – MI Risk Stratification

• The goal is to identify patients who are at high risk for

subsequent cardiac events and who might benefit
from revascularization.
• Initial evaluation involves noninvasive testing:
Submaximal exercise stress testing is generally
performed in stable patients before hospital discharge
to detect residual ischemia and ventricular ectopy
and to provide a guideline for exercise in the early
recovery period.
• Evaluation of LV systolic function, is done using
echocardiography
• High risk patients: those with impaired systolic
function, large areas of ischemic myocardium on
stress testing or postinfarction angina, or ventricular
ectopy
• Post-STEMI patients with LV dysfunction (LV ejection
fraction <40%) are at increased risk of sudden cardiac
death from ventricular arrhythmias.

F. Secondary Prevention of Ischemic Heart Disease

• Smoking cessation reduce risk by 50%

• Antiplatelet agents such as aspirin and clopidogrel
reduce the risk of thrombus formation
• beta-blockers reduce myocardial oxygen demand -
may help suppress ventricular arrhythmias
• Cholesterol-lowering agents such as statins reduce
the number of coronary events and prolong survival.
CAD should have LDL < 70mg/dL
• Angiotensin-converting enzyme Inhibitor (ACE I)
given to all patients after STEMI and to patients with
impaired systolic function ejection fraction <40%,
Diabetes, Hypertension

References

Toy, E., & Patlan, J. (2017). Case Files Internal Medicine.

United States: McGraw-Hill Education.

Ppt. Doc Magnolia Reyes. 2020

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 Prelims (1st Sem) Acute Myocardial Infarction
Dr. Magnolia Reyes
PATHOLOGY· September 11, 2020

V. Appendix A
CARDIAC BIOMARKERS
CARDIAC BIOMARKER DESCRIPTION RISES ELEVATED/ RETURNS TO NORMAL
Creatine phosphokinase ✓ Found in skeletal muscle Rises within 4 to 8 Returns to normal by 48 to 72 hours
(CK) and other tissues hours
✓ Creatine kinase
myocardial band
(CK_MB) more specific
for myocardial injury
Cardiac- specific troponin I ✓ Preferred markers for Rise Cardiac- specific troponin I levels may remain
(cTnI) myocardial injury approximately elevated for 7 to 10 days
Cardiac- specific troponin T ✓ Very sensitive and fairly from 3 to 5 hours cTnT levels for 10 to 14 days
(cTnT) specific indicators of after infarct
myocardial injury, may be
elevated with even small
amounts of myocardial
necrosis
✓ Two sets of normal
troponin levels 6 to 8
hours apart exclude MI

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 Prelims (1st Sem) Acute Myocardial Infarction
Dr. Magnolia Reyes
PATHOLOGY· September 11, 2020

Appendix B
Algorithm for Assessment and Treatment of Chest Pain

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